Objective:To monitor the blood pressure in pediatric patients with coarctation of the aorta (CoA) before and 8 years after surgery, and explore the mechanism of elevated blood pressure in pediatric patients with repaired CoA.Methods:A cohort of 23 pediatric patients who underwent CoA repair between January 2010 and October 2010 in Guangzhou Women and Children's Medical Center was studied. And 20 age-, sex-match patients with isolated ventricular septal defect (VSD) who underwent surgery at the same time, 20 age-, sex-match health patients with normal echocardiographic findings were included in the study. Systolic blood pressure (SBP), diastolic blood pressure (DBP), arm-leg SBP gradient, right carotid intima-media thickness (CIMT), serum transforming growth factor-β1 (TGF-β1) were monitored at baseline(1 day before surgery) and 8-year follow-up (8 years after surgery).Results:There were no differences in SBP and DBP among patients with CoA, patients with VSD and health children at baseline ( P>0.05). But at 8-year follow-up, 2 patients with CoA exhibited hypertension. Not only that, patients with CoA had higher SBP than patients with VSD and health children at 8-year follow-up ( P<0.05). Patients with CoA had higher arm-leg SBP gradient than patients with VSD and health children at baseline ( P<0.01). But there were no differences in arm-leg SBP among patients with CoA, patients with VSD and health children at 8-year follow-up ( P>0.05). Patients with CoA had increased CIMT and higher serum levels of TGF-β1 at baseline and 8-year follow-up ( P<0.05). The preoperative levels of CIMT and serum TGF-β1 in the patients with CoA were highly positively correlated with their levels at 8-year follow-up, respectively ( P<0.01). There was a strong correlation between the levels of CIMT and serum TGF-β1 in patients with CoA, both preoperatively and postoperatively ( P<0.01). The preoperative and postoperative levels of CIMT and serum TGF-β1 in the patients with CoA were highly positively correlated with SBP at 8-year follow-up, respectively( P<0.05). Conclusion:Although surgery can successfully cure the anatomical " stenosis" , patients with CoA have elevated systolic blood pressure than normal people and patients with simple congenital heart disease (such as VSD). And some of the patients with CoA suffer from hypertension at long-term follow-up, even they are normotensive preoperatively. It may be related to vascular remodeling, in which TGF-β signaling pathway may be involved. Monitoring CIMT and TGF-β1 in patients with CoA preoperatively may be significative for prediction for the levels of SBP postoperatively.

This study was aimed to compare the differences of adhesion properties of endothelial cells (EC) from arteries (AEC), veins (VEC) and capillaries (MVEC) under shear stress condition, and to explore whether they can get the same adhesive ability as graft in similar shear stress conditions. With mended parallel plate flow apparatus and peristalsis pump providing fluid shear stress used, endothelial culture models were established in vitro with the same environmental factors as steady culture. To compare the adhesion among three kinds of endothelial cells under dynamic condition and static condition, the dynamic change of cytoskeletal actin filaments and the effects of different adhesive proteins coated on the adhesion of EC to the glass were studied. The cultured endothelial cells under flow conditions were extended and arranged along the direction of flow. The adhesive ability from high to low under static condition were AEC, MVEC and VEC (VEC compared with AEC or MVEC, P < 0.05), sequentially. The adhesion of endothelial cells from variety sources under dynamic culture condition was significantly increased than that of the static groups. The ratio of cell retention was not significantly different between AEC and MVEC. But VEC was significantly different (P < 0.05) compared with AEC or MVEC. The actin filaments (F-actin) were bundled together and arranged along the direction of flow after fluid culture. Dense peripheral band (DPB) gradually disappeared and distinct stress fibers were formed, which even interconnected to form a whole in the MVEC. The adhesion of AEC, VEC and MVEC under shear stress conditions are more significantly increased than those under the static culture conditions, and the MVEC can achieve the same adhesion as AEC.
Arteries ; cytology ; Capillaries ; cytology ; Cell Adhesion ; Cell Culture Techniques ; methods ; Cells, Cultured ; Cytoskeleton ; physiology ; Endothelial Cells ; cytology ; physiology ; Humans ; Shear Strength ; Stress, Mechanical ; Veins ; cytology

The present paper is to research the expression level of the mRNA of scavenger receptor class B type 1-receptor of high-density lipoprotein in endothelial cells after being treated by different shear stress. The second to fourth generations of the cultured human umbilical vein endothelial cells (HUVECs) were used in the experiment. The cells were divided into two groups. The first group was the control group which was not dealt with shear stress; the second group was the experimental group which concluded low shear stress group (4.2 dyne/cm2), moderate shear stress group (8.4 dyne/cm2) and high shear stress group (15 dyne/cm2). The load time was 1h, 2h, 4h and 8h, respectively. Harvesting the cells and extracting total RNA after being treated by different shear stresses, the expression level of the SR-B1 mRNA was detected by semi-quantitative RT-PCR technic. It was found that the expression of SR-B1 mRNA became weaker and weaker compared to the control group when it was stimulated continuously by the low shear stress, the lowest expression of SR-B1 mRNA appeared at 8h. In the moderate shear stress group, the expression of SR-B1 mRNA increased obviously. Compared to the control group, there was significant difference after being treated with 2h. In the high shear stress group, the expression of SR-B1 mRNA increased immediately when it was stimulated by the shear stress. And the expression of SR-B1 mRNA arrived peak value at 4h. Compared to the control group, there was significant difference after being treated for 1h. It was concluded that the harmful mechanism of the low shear stress is that it can increase the incidence of the atherosclerosis by reducing the reverse cholesterol transport and endothelial protection through decreasing the expression of the SR-B1. Otherwise, the high shear stress prevent the genesis of atherosclerosis by the contrary mechanism.
Atherosclerosis ; etiology ; Cells, Cultured ; Human Umbilical Vein Endothelial Cells ; cytology ; metabolism ; Humans ; RNA, Messenger ; genetics ; metabolism ; Scavenger Receptors, Class B ; genetics ; metabolism ; Stress, Mechanical

Objective To evaluate the method of low-intensity anticoagulation therapy in the pregnant women who had received mechanical heart valve replacemant, and the effects of warfarin on the pregnant women and their fetus. Methods This retrospective study involved 56 pregnant women( 61 pregnancies)who had received mechanical heart valve replacement.Their pregnant status, delivery, and anticoagulation therapy were observed and followed-up between May 1986 and November 2009 at West China Hospital of Sichuan University. Results All patients took oral anticoagulant (warfarin) throughout pregnancy. The dose of domestic warfarin was ( 3.02 ± 0.85 ) mg/d ( in 42 cases), and the dose of imported warfarin was (2.84 ± 0.57 )mg/d (in 14 cases). The mean INR value of 401 samples from patients was 1.67 ±0.58. No thromboembolism or major hemorrhagic complications occurred. Minor bleeding occurred in 11 pregnancies. Forty-seven patients had term delivery, 7 had premature birth, 6 had spontaneous abortion, and 1 had intrauterine fetal death. Six newborns were born with low birth weight (2.3 ± 0. 5 ) kg, and no abnormal fetus was observed. Conclusion The low-intensity anticoagulation therapy with warfarin (at a dose of less than 5 mg/d) and a INR target of 1.5 to 2.0 was safe and convenient for the pregnant women,who had received mechanical heart valve replacement. The abnormalities rate of fetus was low.

Lining the inner surface of the walls of blood vessels, Endothelial cells (ECs) go beyond providing selective membrane to maintain the natural structure and function of vessels; they also synthesize varieties of vasoactive proteins to modify the pressure shift in the local flow field and hence they adapt the physiological activities of vessels. In this experiment, ELISA and RT-PCR technologies were adopted. We set up five different pressure loaded ECs groups,one non-activated cultured ECs group and one single shear stress loaded ECs group. Such a design was intended to demonstrate the effects of pressure shift on the expression of vasoactive protein synthesized by ECs [Endothelin-1(ET-1), endothelial Nitric Oxide Synthase (eNOS), Cyclooxygenase-2(COX-2) and Vascular Endothelial Growth Factor(VEGF)]. Our aim was to elucidate the mechanism of the pressure shift mediated dysfunction in ECs and the related dose-effect relationship. Based on these data, we suggest that ECs could modify the expression of vasoactive protein for adapting to the pressure shift in the local flow field; while in the process of--40 cmH2O induced ECs' dysfunction, the vasoactive proteins eNOS, COX-2 and VEGF play an important role in protecting ECs.
Cells, Cultured ; Cyclooxygenase 2 ; genetics ; metabolism ; Endothelial Cells ; metabolism ; physiology ; Endothelin-1 ; genetics ; metabolism ; Humans ; Nitric Oxide Synthase Type III ; genetics ; metabolism ; Pressure ; RNA, Messenger ; genetics ; metabolism ; Vascular Endothelial Growth Factor A ; genetics ; metabolism

The changes of pressure in local circulation flow field and the alterations of biorheological characteristics in Endothelial cells (ECs) would follow the geometric changes of cardiovascular wall structures and would further result in distinct pathophysiological changes of endothelial cellular proliferation and vitality. This experiment is designed to observe the effects of pressure shift on ECs proliferation, apoptosis, and expression of apoptosis-associated protein, to elucidate the influences of pressure shift on the vitality of ECs, and to shed light on the dose-effect relationship concerned. By adopting flow cytometery, transmission electron microscopy, real-time RT-PCR and Western blotting, we set the levels of pressure loading ECs groups and set down the non-activated cultured ECs,single shear stress loading ECs as the control group for studies on the ultra-structure alterations, on the distribution of cell cycle and the changes of proliferation and apoptosis in ECs. We also investigated the changes of the expression of Caspase-3 gene and the changing regularity of P53, Bcl-2 and Fas protein at the translation level. When ECs being exposed to decreased pressure shift (-40 cmH2O), distinct apoptosis in ECs could be observed and a pattern of duration-dependence was seen. The expressions of P53, Bcl-2 and Fas proteins are essential for regulating the genesis and process of ECs apoptosis induced by -40 cmH2O pressure.
Apoptosis ; physiology ; Apoptosis Inducing Factor ; metabolism ; Caspase 3 ; metabolism ; Cell Proliferation ; Cells, Cultured ; Endothelial Cells ; cytology ; Fas Ligand Protein ; metabolism ; Humans ; Pressure ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rheology ; Stress, Mechanical ; Tumor Suppressor Protein p53 ; metabolism ; Umbilical Veins ; cytology

Objective Recent.studies have found a strong association of insulin resistance, which might occur during ischemia reperfusion in vitro in the experimental dogs, with disturbed function of cardiomyocytes. Obvious acute insulin resistance, along with glucose dysmetabolism in the reperfused cardiomyocytes, was furher observed in the study performed with ischemia-reperfused ventric- ular myocytes of rats. We tried to investigate preliminarily the molecular mechanisms of insulin resistance in the cardiomyocytes after ischemia reperfusion. Methods An experimental model of insulin-stimulated ischemia reperfusion (SI/R) was created by isolating cardiomyocytes from adult rats. Glucose uptake of the cardiomyoctyes was evaluated with isotope-labeling technique. Glucose trans- porter 4 (GLUT4) translocation induced by insulin was investigated with Western blot analysis, and the intracellular level of free Ca2+ ([Ca2+]I) was measured quantitatively with Ca2+ indicator Fura-2. Results Insulin can stimulated glucose uptake by cardiomyo- cytes, indicating that these cells were insulin-sensitive. Cardiomyocytes were demonstrated notable acute insulin resistmce during reperfusion. Insulin-stimulated GLUT4 translocation in the cardiomyocytes 15 minutes after reperfusion was 72.2% of that in the con- trol group(P<0.05), in which the GLUT4 content in plasma membrane remained unchanged. The finding suggested that a disturbed GLUT4 translocation might happen in the cardiomyocytes during insulin-stimulated ischemia-reperfusion. Calcium overload was identi- fied in the cardiomyocytes with ischemia reperfusion. At 15 minutes of reperfusion, [Ca2+]I was significantly higher in the reperfused cardiomyocytes than that in the control cardiomyocytes[(318.66±23.06)vs(130.70±0.82) nmol/L, P<0.05], and kept at a higher level [(177.79±17.46) nmol/L] at 60 minutes of reperfusion (P<0.05, vs control). Partial correlation analysis revealed a negative correlation of[Ca2+]I with insulin-induced ghcose uptake in the cardiomyoctyes (r = -0.557,P=0.006). Conclusion Disturbed GLUT4 translocation and decreased intrinsic activity may be important molecular mechanisms for the development of insulin resistance in the cardiomyocytes of rat during insulin-simulated ischemia reperfusion,. [Ca2+]I overload may account for the de- creased intrinsic activity d GLUT4.

This study was conducted to modify the method for establishing the model of myocardial infarction by ligation of the left anterior descending branch (LAD) of coronary artery in rats, and then observations on them were made with the use of electrocardiography, heart function exam and histomorphology. 30 adult male inbred strain Wistar rats were randomly divided into two groups: sham group (n = 5) and model group (n = 25). Each rat in the model group underwent a ligation of the left anterior descending branch. Subsequently, the two groups were compared by use of electrocardiography, heart function and histomorphology. The results have demonstrated that, after being improved, the ligation of the left anterior descending branch of coronary artery is a good method to establish the stable model of myocardial infarction. It can be applied to the research in mechanism and treatment of myocardial infarction.
Animals ; Coronary Vessels ; surgery ; Disease Models, Animal ; Ligation ; methods ; Male ; Myocardial Infarction ; etiology ; Random Allocation ; Rats ; Rats, Wistar

Objiective To evaluate the effect of pearventricular device closure of non-muscular ventricular defercts(VSDs) in infants.Methods From April 2007 to February 2008,39 patients with non-muscular VSDs were received off pump surgical treatment,perventricular device closure were for all the patients.There were 16 males and 23 females with mean age of(14.5±7.8) months(12 to 36 months and mean weight of(12.4±2.3)kg(8.5 to 18.0 kg).There were 34 perimembranous and 5 subateria VSD.The diameter of defects were 3.0 to 11 mm[mean(6.1±2.0)mm].Results Thirty-seven(94.9%)VSDs ere successfully closed,while two were repaired under cardiopulmonary bypass(CPB)instead of device closure because of the complication of moderat aortic reurgitation.The diameter of occluders were 4 to 12mm[mean(8.2±2.0)mm].The tricuspid regurgitations decareasded after operation in 3 patients with perimenmbranous VSDs,while the closure caused new mild or trace tricuspid regurgitations in 8 patients.Six patients with perimembranours VSDs acquired the incomplete right bundle branch blocks affter device closure.The length of hospital stay was 3 to 5 days[mean(3.4±0.4)]after operation and no petient had blood transfusion.Conclustion Perventricular device closure is probably an effective and safe treatment for non-muscular VSDs in unfants.

In mankind, the circulation system is a closed pressure-loaded system; the pressure in circulation flow field would change with the variation of natural or pathological geometry of the local bloodvessel, and the pressure shift induced by the variation of vascular geometry would lead to a series of physiological and pathological changes in the endothelial cells (ECs). This experiment is designed to elucidate the effects of different pressure shift on F-actin alignment and expression in cultured endothelial cells in vitro, and to investigate the relationship between the altered pressure shift and the expression intensity of Vascular adhesion molecule (VCAM) and Integrin alphaVbeta3. Non-activated cultured ECs and single shear stress loaded ECs as control group were set, the double-immuno-fluoro-cytochemistry, laser confocal scanning microscopy and image analysis system were used to observe the expression of VCAM, Integrin alphaVbeta3 and F-actin in endothelial cells which were exposed to levels of pressure shift in an improved parallel plate flow chamber. When exposed to different decreased pressure shift, the expression intensity of VCAM, Integrin alphaVbeta3 and F-actin showed regular changes. The decreased pressure shift resulted in changes in cell alignment and cytoskeleton F-actin, and also affected ECs adhesion function and transmembrane mechanotransduction function which were represented by VCAM and Integrin alphaVbeta3 respectively.
Actins ; genetics ; metabolism ; Cell Adhesion ; Cells, Cultured ; Endothelial Cells ; cytology ; metabolism ; Hemodynamics ; Humans ; Integrin alphaVbeta3 ; genetics ; metabolism ; Pressure ; Umbilical Veins ; cytology ; Vascular Cell Adhesion Molecule-1 ; genetics ; metabolism